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At least 19 recordsLinked to original sources
PubMed1996

Cell surface-associated extracellular distribution of a neural proteoglycan, 6B4 proteoglycan/phosphacan, in the olfactory epithelium, olfactory nerve, and cells migrating along the olfactory nerve in chick embryos.

The immunocytochemical and immuno-electron microscopic distribution of a neural proteoglycan (PG) was investigated with a monoclonal antibody, MAb 6B4, in the olfactory epithelium, the olfactory nerve, and the cells originating the epithelium and migrating along the olfactory nerve toward the forebrain in chick embryos. The PG recognized by MAb 6B4, that is 6B4 PG, in the brain of early postnatal rats, is identical to phosphacan. In chick embryos, immunoreactivity to 6B4 PG appeared on embryonic day (ED) 3-3.5 in a thin layer beneath the olfactory epithelium. It disappeared immediately, then becoming apparent in the bundles of the olfactory nerve. The immunoreactivity in the nerve bundles gradually increased during ED 5-11. On the other hand, cell surface-associated extracellular localization of the immunoreactivity was seen in the olfactory epithelium on ED 6 and afterwards. Immunofluorescent double-labeling of 6B4 PG and gonadotropin-releasing hormone (GnRH) revealed that the cell bodies of both GnRH-containing cells and other cells migrating along the olfactory nerve were surrounded by a rim immunoreactive to the PG. Under an electron microscope, the surfaces of the cell bodies and of the neurites in the nerve bundles were surrounded by deposits immunoreactive to 6B4 PG. These results indicate that 6B4 PG in chick embryos is one type of cell surface-associated extracellular matrix molecule, and that 6B4 PG covered the surfaces of migrating cells and of elongating olfactory nerve. The cell surface-associated extracellular localization of 6B4 PG found in the nasal region, taken together with the binding properties of this PG with cell adhesion molecules shown in rat brains, suggested that 6B4 PG played a role in guiding the migration of cells along the olfactory nerve in chick embryos.

Animals↗
PubMed2001

Volumetric and horseradish peroxidase tracing analysis of rat olfactory bulb following reversible olfactory nerve lesions.

Olfactory receptor neurons can regenerate from basal stem cells. Receptor neuron lesion causes degenerative changes in the olfactory bulb followed by regeneration as new olfactory receptor axons innervate the olfactory bulb. To our knowledge, parametric analyses of morphometric changes in the olfactory bulb during degeneration and regeneration do not exist except in abstract form. To better characterize olfactory bulb response, we performed morphometric analysis in rats following reversible olfactory nerve lesion with diethyldithiocarbamate. We also performed anterograde tracing of the olfactory nerve with wheatgerm agglutinin linked to horseradish peroxidase. Results of morphometry and tracing were complementary. The glomerular layer and external plexiform layer showed shrinkage of 45 and 26%, respectively, at 9 days. No significant shrinkage occurred in any other layer. Individual glomeruli shrank by 40-50% at 3 and 9 days following lesion. These data show that degenerative changes occur both in the glomeruli and transneuronally in the external plexiform layer. Olfactory nerve regeneration (identified by WGA-HRP transport) paralleled volumetric recovery. Recovery occurred first in ventral and lateral glomeruli between 9 and 16 days followed by recovery in medial and dorsal glomeruli. These data indicate substantial transynaptic degeneration in the olfactory bulb and a heretofore unrecognized gradient in olfactory nerve regeneration that can be used to systematically study recovery of a cortical structure.

Animals↗
PubMed1998

LHRH neurons migrate into the trigeminal nerve when the developing olfactory nerve fibers are physically interrupted in chick embryos.

Most LHRH neurons actively migrate from the olfactory epithelium to the forebrain during embryonic days (ED) 3.5-8. When a small piece of the membrane filter was placed on the central course of the olfactory nerve in ED 3.5-5 chick embryos, LHRH neurons deviated from their regular migratory course at ED 6.5-7.5 to follow a route along the PSA-NCAM-positive medial and lateral nasal branches of the ophthalmic nerve of the trigeminal nerve. The olfactory nerve fibers which were specifically immunoreactive for somatostatin also deviated into the ophthalmic nerve. Enzymatic removal of PSA using endoneuraminidase did not interfere with the migration of LHRH neurons into the ophthalmic nerve bundle of the trigeminal nerve. The presence of structural supports seems to be primarily of importance in the migration of LHRH neurons along the olfactory and trigeminal nerve bundles. PSA may be less important for the migration of the LHRH neurons along peripheral neural elements.

Animals↗
PubMed2001

Dopamine D2 receptor-mediated presynaptic inhibition of olfactory nerve terminals.

Olfactory receptor neurons of the nasal epithelium project via the olfactory nerve (ON) to the glomeruli of the main olfactory bulb, where they form glutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the olfactory bulb, and with juxtaglomerular interneurons. The glomerular layer contains one of the largest population of dopamine (DA) neurons in the brain, and DA in the olfactory bulb is found exclusively in juxtaglomerular neurons. D2 receptors, the predominant DA receptor subtype in the olfactory bulb, are found in the ON and glomerular layers, and are present on ON terminals. In the present study, field potential and single-unit recordings, as well as whole cell patch-clamp techniques, were used to investigate the role of DA and D2 receptors in glomerular synaptic processing in rat and mouse olfactory bulb slices. DA and D2 receptor agonists reduced ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells. Spontaneous and ON-evoked spiking of mitral cells was also reduced by DA and D2 agonists, and enhanced by D2 antagonists. DA did not produce measurable postsynaptic changes in juxtaglomerular cells, nor did it alter their responses to mitral/tufted cell inputs. DA also reduced 1) paired-pulse depression of ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells and 2) the amplitude and frequency of spontaneous, but not miniature, excitatory postsynaptic currents in juxtaglomerular cells. Taken together, these findings are consistent with the hypothesis that activation of D2 receptors presynaptically inhibits ON terminals. DA and D2 agonists had no effect in D2 receptor knockout mice, suggesting that D2 receptors are the only type of DA receptors that affect signal transmission from the ON to the rodent olfactory bulb.

Animals↗
PubMed1994

Neuropeptide tyrosine is expressed in ensheathing cells around the olfactory nerves in the rat olfactory bulb.

The olfactory bulbs of young and adult normal rats and of colchicine-treated rats and of some other species were analysed for the presence of neuropeptide Y and neuropeptide Y messenger RNA, using immunohistochemistry at the light- and electron-microscopic levels and with in situ hybridization. In the rat and mouse, but not in monkey and guinea-pig, neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA were observed in ensheathing cells in the olfactory nerve layer of the olfactory bulb and within nerve bundles in the olfactory mucosa. Double staining experiments revealed that neuropeptide Y-like immunoreactivity was often present in a restricted compartment, mainly the Golgi apparatus, of S-100 protein-positive ensheathing cells. After colchicine treatment a different distribution of neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA was observed. Thus, in the outer olfactory nerve layer both neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA disappeared, whereas in the inner part messenger RNA levels remained high and neuropeptide Y-like immunoreactivity was observed in many granule-like structures distributed diffusely in the cytoplasm. The present findings suggest that neuropeptide Y may be involved in the control of regeneration, growth and/or guiding of the axons of the olfactory sensory neurons, the only mammalian neurons known to have a continuous renewal and growth during adult life.

Animals↗
PubMed1997

Glomerular synaptic responses to olfactory nerve input in rat olfactory bulb slices.

In olfactory bulb slices from young rats, the field potential evoked in the glomerular layer by stimulation in the olfactory nerve layer consisted of two negative components: an early component (N1) which was blocked by bath application of the kainate/amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), and a late, prolonged component (N2; duration > or = 350 msec) which was unaffected by CNQX, was enhanced by reduction of Mg2+ in the medium, and was blocked by the N-methyl-D-aspartate receptor antagonist DL-2-amino-5-phosphonovalerate (50 microM). A comparison of the glomerular field potentials before and after knife cuts that isolated the glomerular layer from the deeper layers of the olfactory bulb indicated that both N1 and N2 were produced by currents generated, for the most part, within the glomeruli. A laminar analysis of the field potential profiles evoked by olfactory nerve stimulation in standard medium, or in the presence of CNQX, showed that N1 and N2 reversed polarity in the external plexiform and mitral cell layers, suggesting that both components reflected synaptic responses in the distal, apical dendrites of mitral/tufted cells. Simultaneous field potential recordings in the glomerular layer and intracellular recordings in the mitral cell layer showed that: (i) N1 is associated with a brief, short-latency spiking activity of mitral cells, and (ii) N2 is associated with prolonged mitral cell spiking, since N2 and the late cell firing had similar time-courses, and both were blocked by bath applied DL-2-amino-5-phosphonovalerate. Application of the GABA(A) receptor antagonist bicuculline methiodide (10 microM) to standard medium selectively enhanced N2. The enhanced N2 was significantly reduced by DL-2-amino-5-phosphonovalerate. Strychnine, an antagonist of glycine receptors, had similar effects to those of bicuculline, but only at high concentrations that have been previously shown to block GABA(A) receptors; at low concentrations strychnine had no effect. The effects of all drugs tested were reversible. In the rat olfactory bulb, activation of the olfactory nerve evokes a kainate/AMPA receptor-mediated response in the distal, apical dendrites of mitral/tufted cells, followed by a slow N-methyl-D-aspartate receptor-mediated response which triggers prolonged discharge of mitral cells. GABA(A) receptor-mediated inhibition appears to suppress, preferentially, this N-methyl-D-aspartate receptor-mediated component. The presence of prolonged N-methyl-D-aspartate receptor-mediated postsynaptic activity at the primary synapses of the olfactory system may play a key role in olfactory processing by facilitating synaptic integration and plasticity.

Animals↗
PubMed1994

Recovery of olfactory behavior. I. Recovery after a complete olfactory bulb lesion correlates with patterns of olfactory nerve penetration.

The olfactory system is an excellent system in which to study issues related to potential functional recovery after a debilitating brain injury. The olfactory system is well-characterized, easily accessible and there are a vast number of studies available from a variety of perspectives. The experimental aim of this research is to examine the anatomical correlates associated with potential behavioral recovery in rats that receive complete olfactory bulb lesions as neonates or as adults. The results show that behavioral recovery occurs only when olfactory nerve penetration of the central nervous system is observed. Further, both olfactory nerve penetration and behavioral recovery are age-dependent phenomena. The olfactory nerve penetration only occurs when the olfactory bulb lesion is performed in neonates. Behavioral recovery of olfactory ability follows a linear trend and reaches near normal levels during the six weeks behavioral testing period. Histological analysis using an antibody for olfactory marker protein (an olfactory nerve-specific marker) reveals two potential candidates for the anatomical pathway responsible for behavioral recovery: olfactory nerve to orbital frontal cortex and olfactory nerve to olfactory peduncle. This report presents evidence that recovery of olfactory ability can occur in the absence of the olfactory bulb if the lesion is performed when the rat is still a neonate.

Animals↗
PubMed1998

TrkA expression in mouse olfactory tract following axotomy of olfactory nerves.

The olfactory bulb is one of the brain regions that synthesizes the nerve growth factor (NGF). Functional roles of the bulbar NGF remain to be determined. The aim of the present study was, using an antibody specific to the high-affinity NGF receptor (trkA), to examine immunohistochemically the distribution of the NGF receptor in the mouse olfactory tract, under normal conditions and during regenerative processes. In normal mouse olfactory epithelia, trkA immunoreactive cell bodies were only seen in basal cells. Cell bodies of olfactory receptor cells did not express trkA immunoreactivity, but their neuronal processes (olfactory nerve fibres and bundles in the olfactory mucosa and the olfactory bulb) displayed trkA immunoreactivity. After axotomy of olfactory nerves, regenerating olfactory cells (basal cells and olfactory receptor cells) expressed trkA immunoreactivity in intramucosal and intrabulbar neuronal processes of olfactory receptor cells. These results suggest involvement of the bulbar NGF in the process of synaptogenesis and/or regeneration of the olfactory nervous system.

Animals↗
PubMed1985

Immunohistochemical study of subclasses of olfactory nerve fibers and their projections to the olfactory bulb in the rabbit.

The organization of the olfactory nerve projection to the olfactory bulb was studied immunohistochemically in the rabbit by using monoclonal antibodies (MAbs). Out of 42 MAbs raised against the homogenate of the olfactory bulb, two types of MAbs that strongly stained the olfactory nerve fibers (axons of olfactory receptor cells) were selected and their staining patterns were analysed in detail. MAbs of one type (represented by MAb R2D5) specifically labeled all olfactory receptor cells in the nasal epithelium and all olfactory nerve fibers and their terminal portions in the bulb. The other type of MAbs (represented by MAb R4B12) recognized only a subgroup of olfactory nerve fibers. The R4B12-positive fibers were distributed over the ventrolateral areas but not in the dorsomedial areas of the epithelium. Similarly in the bulb, the R4B12-positive fibers terminated in the glomeruli in the ventrolateral and the caudal regions but not in the dorsomedial region. These results demonstrate for the first time the cellular heterogeneity among olfactory receptor neurons at the molecular level. The segregated distribution of the subtypes of olfactory receptor cell axons both in the epithelium and the bulb indicates a defined topographical organization of the olfactory nerve projection. These results also suggest a functional division between dorsomedial and ventrolateral areas both in the epithelium and the bulb.

Afferent Pathways↗
PubMed1993

Purification of olfactory nerve ensheathing cells from the olfactory bulb.

Cells of the olfactory nerve layer of the olfactory bulb are labeled with the O4 antibody, which also labels Schwann cells, oligodendrocytes, and many oligodendrocyte-type-2 astrocyte (O-2A) progenitors. Purification of cells which were O4+, but did not express galactocerebroside (GC), from spinal cord, hippocampus, corpus callosum, and cerebellum of perinatal rats always yielded cells with the expected characteristics of O-2A progenitors. In contrast, the great majority of O4+GC- cells isolated from the olfactory bulb expressed an antigenic phenotype and pattern of differentiation in vitro which did not correspond with that of any previously described glial populations. As the localization of O4 staining in the olfactory bulb indicates that these cells are olfactory nerve ensheathing cells (ONECs), our results therefore suggest that ONECs represent a novel glial cell-type which can now be analyzed as a purified population.

Animals↗
PubMed1992

Monoclonal antibody immunohistochemistry of a temporal relationship between axonal elimination of aberrant olfactory nerves and synaptogenesis in the rabbit olfactory bulb during middle embryonic periods.

Immunostaining using olfactory nerve- and synaptic vesicle protein-specific monoclonal antibodies revealed their characteristic appearance in the rabbit olfactory bulb during prenatal development. Prior to formation of glomeruli, olfactory nerve fibers extended beyond their target region deep into the bulb zones. Subsequently the aberrant axons decreased in number, and correspondingly, synaptic vesicle protein occurred in the innermost region of the olfactory nerve layer. It is concluded that the lack of synaptogenesis causes axonal elimination of aberrant olfactory nerves. Present results support the hypothesis that supernumerary axons degenerate unless synaptic contacts are secured; the olfactory nerves must arrive at the appropriate terminal zone in the glomeruli.

Animals↗
PubMed1988

Slow transport in a nerve with embryonic characteristics, the olfactory nerve.

The kinetics for slowly transported polypeptides have been examined in intact garfish olfactory nerves. The shape of the slow peak is essentially determined by alpha-and beta-tubulin which are by far the major polypeptides of the entire wave. The proximal area of the peak is similar to the slow component a (Sca) subcomponent defined in other nerves and contains discretely moving neurofilament proteins. The distal peak area, however, is more reminiscent of Scb. The two subcomponents were found to overlap considerably. Traces of polypeptides comigrating with tubulin and actin move far ahead of the slow wave at rates similar to the rate of slow transport measured in growing fibers and to the maximal velocity of axonal elongation. One of the most striking properties of slow transport in this nerve is the difference in the spreading of the various transported polypeptides along the axon, following their release from the perikarya. Labeled tubulin and actin can cover more than 20 cm of nerve; while neurofilament proteins can be found only on a 6 cm segment. Comparisons between slow transport in garfish olfactory axons and other vertebrate nerves indicate that despite major differences, the basic characteristics of slow transport are conserved. The features specific to the olfactory nerve may reflect its specialized properties. The constant turnover of olfactory neurons implies that these cells have an excellent growth potential but a short life span and, therefore, never reach full maturity. It can, therefore, be expected that their molecular composition is reminiscent of that embryonic neurons with a high level of plasticity but a slow stability.

Animals↗
PubMed1994

Evidence for GABAB-mediated inhibition of transmission from the olfactory nerve to mitral cells in the rat olfactory bulb.

The GABAB agonist baclofen blocks transmission from the olfactory nerve to second order neurons in the frog olfactory bulb, and GABAB receptors in the rat olfactory bulb are selectively located in the glomerular layer. A reasonable hypothesis, therefore, is that inhibition in the glomerular layer is mediated, at least in part, by GABAB receptors. Here, we investigated the role of GABAB receptors in regulating the responses of mitral cells to activation of the olfactory nerve in the rat. Topical application of baclofen to the surface of the rat olfactory bulb reduced the amplitude of field potentials evoked by olfactory nerve stimulation (orthodromic response). Baclofen reduced the orthodromic response in a dose-dependent manner but the drug had no effect on the field potential evoked by antidromic activation of mitral cell axons (antidromic response). Baclofen also reduced olfactory nerve-evoked responses of mitral cells in an olfactory bulb slice preparation. The pharmacological specificity of the inhibition was confirmed by showing that the GABAB antagonist, CGP 55845A, blocked the inhibitory action of baclofen. These results suggest that transmission from olfactory nerve terminals to second order neurons is negatively regulated by periglomerular GABAergic interneurons; this inhibition is mediated, at least partially, by GABAB receptors.

Animals↗